Multiple viral infections in a group of intravenous drug users: hepatitis B virus exposure is the risk factor

A matched nested case–control study of 33 paired cases and controls was conducted, based on a study cohort in Long An county, Guangxi, China, to determine whether infection with hepatitis B virus (HBV) with pre-S deletions is independently associated with the development of hepatocellular carcinoma (HCC), without the confounding effects of basal core promoter (BCP) double mutations. The prevalence of pre-S deletions was significantly higher in HCC (45.5 %, 15 of 33) than the controls (18.2 %, 6 of 33) (P<0.01), under the control of the influence of BCP double mutations. Most of the pre-S deletions occurred in, or involved, the 5′ half of the pre-S2 region and the difference between HCC (93.3 %, 14 of 15) and controls (66.7 %, four of six) was significant for this region (P=0.015). There was no significant difference in pre-S deletions between the BCP mutant group and BCP wild-type group (P>0.05), nor was the prevalence of pre-S deletions significantly different between genotypes B and C (P>0.1). These results suggest that pre-S deletions constitute an independent risk factor for HCC and their emergence and effect are independent of BCP mutations. The 5′ terminus of pre-S2 is the favoured site for the deletion mutations, especially in HCC cases. Further prospective studies are required to confirm the role of these mutations in the development of HCC.

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Viral Hepatitis: 1985 Update

Pediatrics in Review ◽

10.1542/pir.7.1.3 ◽

1985 ◽

Vol 7 (1) ◽

pp. 3-11

Author(s):

Saul Krugman

Keyword(s):

Hepatitis B Virus ◽

Hepatitis B ◽

Viral Hepatitis ◽

Hepatitis A ◽

Viral Infections ◽

Hepatitis A Virus ◽

Fatal Outcome ◽

Specific Marker ◽

Hepatitis D ◽

B Virus

During the past two decades extraordinary advances in hepatitis research have clarified the etiology and natural history of the disease. At least four types of hepatitis have been identified: A, B, D (delta), and non-A, non-B. Hepatitis A virus (HAV), hepatitis B virus (HBV), and hepatitis D virus (HDV) have been characterized. Serologic tests have been developed to detect the antigens and antibodies associated with these three hepatitis infections. As of the present time, the non-A, non-B viral agents have not been identified. Therefore, non-A, non-B hepatitis is diagnosed by excluding other viral causes of hepatitis, such as hepatitis A virus, hepatitis B virus, Epstein-Barr virus (EBV), cytomegalovirus (CMV), and others. A recent report indicating that non-A, non-B hepatitis may be caused by a retrovirus, if confirmed, may provide a specific marker of this infection. The course of viral hepatitis is variable; it may be an asymptomatic, anteric infection, or it may be an acute illness characterized by fever, malaise, anorexia, nausea, abdominal pain, and jaundice. Most patients recover completely, but occasionally the infection may be complicated by chronic hepatitis, cirrhosis, and, occasionally, by a fulminant fatal outcome. This review will be devoted predominantly to a discussion of the diagnostic and prophylactic aspects of hepatitis A and hepatitis B viral infections.

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